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HIV for the EDHIV for the ED
Navpreet Sahsi
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Special thanks to Dr. Margriet Greidanus and Dr. James Huffman for their help and allowing use of some of their slides or images for this presentation.
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OutlineOutline• Epidemiology• HIV Basics• HIV in the ED, in the post HAART
ERA• Primer on Needlestick injuries
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EpidemiologyEpidemiologyWorldwide: 59 million persons
infected, with 20 million deaths worldwide.
US – Currently more than one million individuals currently infected, with greater than fourty thousand new patients diagnosed each year
Canada - ???
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How many Canadians have a How many Canadians have a positive HIV Diagnosis? (June positive HIV Diagnosis? (June 2008)2008)
A) 30,000B) 60,000C) 90,000D) 120, 000
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AnswerAnswer
B) 60, 000
Public Health Agency of Canada 2008 Surveillance report.
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http://www.avert.org/canada-hiv.htmhttp://www.avert.org/canada-hiv.htm
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What Province has the What Province has the highest proportion of HIV highest proportion of HIV cases?cases?
A) BCB) AlbertaC) OntarioD) QuebecE) Nunavut
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AnswerAnswer
B) Ontario – currently accounts for 39% of the nations HIV cases
BC, Ontario, Quebec, and Alberta account for 85% of our population, and 95% of our HIV cases
Currently 3 reported HIV positive cases in Nunavut since 2002 (epidemic?)
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HIV BasicsHIV BasicsFrom Wikipedia: “HIV enters……. macrophages and CD4+
T cells by the adsorption of glycoproteins on its surface to receptors on the target cell followed by fusion of the viral envelope with the cell membrane and the release of the HIV capsid into the cell.[74]
[75]Entry to the cell begins through interaction of the trimeric envelope complex (gp160 spike) and both CD4 and a chemokine receptor (generally either CCR5 or CXCR4, but others are known to interact) on the cell surface.[74][75] gp120 binds to integrin α4β7 activating LFA-1 the central integrin involved in the establishment of virological synapses, which facilitate efficient cell-to-cell spreading of HIV-1.[76] The gp160 spike contains binding domains for both CD4 and chemokine receptors.[74][75] The first step in fusion involves the high-…..”
Ummm……..what?
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Better? Better?
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The real basicsThe real basics
HIV – single stranded RNA virusPrimarily attacks host cells involved in
immune function – primarily CD4 T cellsMakes copies into host genome’s DNAHigh viral load early – until immune
system kicks in ◦Accounts for acute symptomatic phase
Slowly weakens immune system -> badness
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How HIV WorksHow HIV WorksHIV
1. Attachment to host cell
2. Reverse transcriptase makes DNA from the virus’s RNA
3. Integration into host cell’s nucleus
4. Reproduction of viral components
5. Assembly of new HIV viruses
6. Release
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BasicsBasicsModes of Transmission
◦Unprotected vaginal or anal intercourse with an infected partner
◦Sharing needles with infected partner
◦Contact with infected blood◦Perinatal transmission
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Virus is passed in infected body fluids◦High concentration in blood, semen, vaginal
fluid and breast milk◦Low levels in almost every other fluid (incl.
sweat, urine, csf, tears, bone marrow, alveolar fluid, synovial fluid, amniotic fluid and saliva small likelihood of transmission
Risk Factors- Viral load (higher load = higher risk)- CD4 count < 200 cells/microL- Other STD’s – especially ulcerative lesions
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Seroconversion (detectable antibody response to HIV)◦Sources vary, but most sources state
that most patients seroconvert to positive HIV serology in 4 to 10 weeks
◦> 95 % within six months◦Median time to exposure 63 d
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Natural HistoryNatural HistoryViral transmissionPrimary HIV infection (acute HIV
infection)SeroconversionClinically latent period (+/-
lymphadenopathy)Early symptomatic HIV infxAIDSAdvanced HIV infx (CD4 < 50)
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Natural History of HIV Natural History of HIV InfectionInfection
0 2 2 4 6
Viral L
oad
CD
4 Count
8 10
weeks years
4 6
Num
ber
of
CD
4 c
ells
/ V
iral
Load
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Natural History of HIV Natural History of HIV InfectionInfection
0 2 2 4 6
Viral L
oad
CD
4 Count
8 10
weeks
Earl
y H
IV
Infe
cti
on
4 6
Num
ber
of
CD
4 c
ells
/ V
iral
Load
Clinical Latent Period
AID
S Ad
van
ced
AID
S
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Acute HIV infectionAcute HIV infectionUsually develop 2 – 4 weeks post
exposure and last for less than 14 days
Presentation is nonspecific and frequently missed◦Diagnosis is missed in up to 75 percent
of patients due to low index of suspicion◦In a small case series from Seattle only
5 of 19 patients (26 %) in HIV surveillance program who sought care from ED’s and walk-in’s were diagnosed with acute HIV infection
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What is the most common What is the most common initial presentation with initial presentation with acute HIV?acute HIV?A) FeverB) PharyngitisC) RashD) HeadacheE) Lymphadenopathy
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A) Fever - > 90%B) Pharyngitis - > 70 %C) Rash – 40- 80 %D) Headache – 30 – 70 %E) Lymphadenopathy – 40 – 70 %
Presentation very similar to flu-like or mononucleosis-like syndrome.
After six months of infection, plasma viremia reaches a steady state
Viral load is most important predictor of progession of disease in early stages
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Natural History of HIV – Natural History of HIV – Clinical Latent PeriodClinical Latent PeriodClinical latent period
◦Generally no findings except for possible lymphadenopathy
◦Persistent generalized lymphadenopathy (PGL) referred to as enlarged lymph nodes involving at least two non-contiguous sites other than inguinal nodes
◦Lymphoid tissue serves as the major reservoir for HIV. Lymphoid tissue traps free virus and infected CD4 T cells
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Natural History of HIV - Early Natural History of HIV - Early symptomatic HIV infectionsymptomatic HIV infection
AIDS indicators – can also occur with other disease processes, but are typically more frequent or more severe with an HIV infection
- Thrush- Vaginal candidiasis that is persistent, frequent, or
difficult to manage- Oral hairy leukoplakia- Herpes zoster involving two episodes or more than one
dermatome- Peripheral neuropathy- Bacillary angiomatosis- Cervical dysplasia- Cervical carcinoma in situ- Constitutional symptoms such as fever (38.5°C) or
diarrhea for more than one month- Idiopathic thrombocytopenic purpura- Pelvic inflammatory disease, especially if complicated by
a tubo-ovarian abscess
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CandidaCandida
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Oral Hairy LeukoplakiaOral Hairy Leukoplakia
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Herpes ZosterHerpes Zoster
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Probability of developing AIDS Probability of developing AIDS within 3 yearswithin 3 years
Pro
babili
ty o
f pro
gre
ssio
n t
o A
IDS
(%)
Viral Load (copies/mL)Ann Intern Med
1997;126:946
(N=1,637)(N=1,637)
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AIDSAIDS
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AIDSAIDS
Diagnosis occurs when a person:1. Has antibodies against HIV in their
bloodAND2. Is diagnosed with one or more AIDS-
defining illnesses
◦ In the US (but not Canada or Europe) the AIDS definition also includes all HIV-infected individuals with a CD4 count lower than 200 cells/μL or a CD4 percentage less than 14%
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What are the opportunistic infections that are considered AIDS –defining illnesses?
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AIDS-Defining IllnessesAIDS-Defining Illnesses
Candidiasis of esophagus, trachea or lungs
Cervical Cancer (invaisive)
Coccidiomycosis Cryptococcosis Cryptosporidiosis Isosporiosis Cytomegalovirus disease HSV (>1month duration) Disseminated
histoplasmosis HIV encephalopathy Kaposi’s sarcoma
Lymphoma (CNS or Burkitt’s)
Mycobacterium avium complex
Mycobacterium tuberculosis (pulmonary)
Pneumocystis pneumonia Recurrent bacterial
pneumonia Progressive multifocal
leukoencephalopthy Recurrent Salmonella
septicemia Toxoplasmosis of the
brain HIV wasting syndrome
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Pneumocystis carinii (PCP)Pneumocystis carinii (PCP)
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TuberculosisTuberculosis
Apical infiltrates
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Kaposi’s SarcomaKaposi’s Sarcoma
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ToxoplasmosisToxoplasmosis
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LymphomaLymphoma
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Natural History of HIV – Natural History of HIV – AIDSAIDS10% of pts will develop an AIDS
defining diagnosis with a CD4 count above 200/mm3
Most common AIDS diagnosis (prior to HAART)◦P. carinii pneumonia - 42.6%◦Esophageal candidiasis – 15%◦Wasting – 10.7%◦Kaposi’s Sarcoma – 10.7%◦Disseminated M. Avium infection -4.8%◦Tuberculosis – 4.5%
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Advanced HIVAdvanced HIVCD4 < 50 Median time of survival 12- 18
months in the absence of ARV’s Presence of end-stage disease –
including disseminated MAC or disseminated CMV
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So learning about advanced HIV/AIDS is great, and we all love looking at pictures of Kaposi’s Sarcomas, but does this even matter anymore?
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http://www.youtube.comwatchv=DGJDzufJKlc
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The HAART EraThe HAART EraRecommended reading
◦Venkat et al. Care of the HIV-Positive Patient in the Emergency Department in the Era of Highly Active Antiretroviral Therapy. Ann Emerg Med. 2008; 52:274-285
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Times have changed…Times have changed…In 80’s hospitalizations in HIV
population were mainly due to opportunistic infections and conditions related to patient’s poor immune response to other pathogens
Primarily in patients under 40 years old
In 1993 33.3 % of HIV-related admissions were due to infections caused by opportunistic infections or uncharacterized pneumonia
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Living Living longer….longer….Now with the success of HAART,
patients are living longerFor a 20 year old HIV-infected patient,
mean life-expectancy has increased from 9.1 years (+/- 2.3 years) in 1993 to 23.6 years (+/- 4.4 years) in 2002
Now illnesses related to cardiovascular disease, medication adverse effects, and malignancies (mainly lymphoma) have become more prevalent
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Who gets HAART?Who gets HAART?Controversial – still debatedFor sure
◦CD4 < 350 cells/microL◦Pregnancy◦HIV – associated nephropathy or
neuropathy◦Co-infection with HBV or HCV
receiving therapy◦History of AIDS-defining illness
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??◦Age > 50◦Discordant couples◦CD4 > 350◦Cardiovascular disese
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HAART drugsHAART drugsLots of fancy drugs that we never
prescribe…Basically 3 major groups
◦Nucleoside reverse transcriptase inhibitore (NRTIs)
◦Non – NRTIs◦Protease inhibitors
◦Plus some new ones that are being used, but beyond the scope of this talk…..
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How NRTI’S WorkHow NRTI’S WorkHIV
Nucleoside reverse transcriptase inhibitors (NRTI’s) latch onto the new strand of DNA that reverse transcriptase is trying to build
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How NNRTI’S WorkHow NNRTI’S WorkHIV
Non-nucleoside reverse transcriptase inhibitors (NNRTI’s) hook onto reverse transcriptase and stop it from working
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How PI’s WorkHow PI’s WorkHIV
Protease inhibitors (PI’s) prevent final assembly and completion of new HIV viruses within the cell
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HAARTHAARTMost patients are on a combination
of drugs from all three classesSide effects many – look up specificsThings of note
◦All ARV’s have potential for hepatotoxicty (any class)
◦Lactic Acidosis◦NNRTI’s and PI’s affect the cytochrome
p450 system – drug interactions!
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Cardiovascular DiseaseCardiovascular DiseaseACS
◦All protease inhibitors cause hyperlipidemia, hyperglycemia and truncal obesity
◦Increased time receiving HAART associated with 26% increased relative risk of MI/year
Take home: Consider HIV positive patients on prolonged ARV therapy at risk for ACS often at younger ages
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What is the most common What is the most common respiratory pathogen in the respiratory pathogen in the post-HAART era?post-HAART era?
A) Pneumocysitis JiroveciB) C. pneumoniaC) Strep pneumoD) LegionellaE) TB
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PulmonaryPulmonaryC) Strep. Pnuemonia most common
pneumonia◦Was PJP in pre-HAART era◦Similar presentation as non-HIV patients◦Can treat similarly if no immune
compromiseHIV is an independant RF for COPD0.5% will have pulmonary
hypertension◦Not related to CD4 count◦Not related to specific HAART therapy
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Pneumocystis Jirvoveci Pneumonia◦Prolonged course (2 weeks)◦Typical symptoms of pneumonia -
nonspecific◦CXR interstitial infiltrates in 80%,
otherwise N◦Treatment is TMP-SMX oral or IV
If oral, start 2 DS tabs q8h
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RenalRenalARF is now a leading cause of
death in HIV-infected patients◦HIV nephropathy = HAART◦Due to HIV mediated viral or
immunologic disease, as well as treatment-related effects
PI’s associated with urolithiasis◦Rx is the same
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CNSCNST. Gondii and C. neoformans were
predominant diseases pre-HAART but less common now
Always CT before LP in workup of new neuro symptoms in patient with prolonged course of HIV infection
Increased risk of CVA – aging population and medication effects
Also think: AIDS dementia, lymphoma, Progressive multifocal leukoencephalopathy (encephalitis)
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Peripheral Nervous Peripheral Nervous SystemSystemDistal sensory neuropathies – both
HIV and HAART related (NRTs)◦Typically hypersensitivities to distal
extremities +/- absent ankle reflexes Discontinue meds and treat with gabapentin
and NSAIDSAcute demyelinating
polyneuropathy◦Presents like Guillain-Barre (ascending
muscle weakness and sensory changes)◦Treated with plasmaphoresis
Chronic relapsing demyelinating polyneuropathy
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GI and LiverGI and Liver Diarrhea – v. common problem
◦ C. Diff is the most likely bacterial pathogen (up to 36% of patients!)
◦ Assess and treat as you would non-HIV patients If advanced AIDS need to think about
cryptosporidium and microrsporidia – need special stool studies
Co-infection with Hep B/C causes most serious hepatic complications◦ 2-3x more likely to develop chronic liver dz◦ Shorter time to progression of AIDS◦ If HAART meds stopped, severe exacerbations of
Hep B can occur ARV’s can cause an increase in all transaminases
and unconjugated bili with no clinical liver disease
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Hematologic and Hematologic and OncologicOncologic Anemia of chronic disease is very common Hemolytic anemia can be severe associated with
certain meds Neutropenia, thrombocytopenia secondary to
disease progression Increased venous thromboembolic events (2-10x
the risk)◦ Coumadin has significant interactions with Protease
inhibitors meds Increased risk of TTP regardless of HAART Increased malignancies – Hodgkin’s, anal cancer,
lung cancer Any person with anal condylomata needs to be
referred for anal cancer screening (HAART hasn’t changed risk)
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EndocrineEndocrineProtease inhibitors increase risk
of hyperlipidemia and truncal obesity◦Increased risk of insulin resistance
and DM
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PsychiatricPsychiatric Depression 40% - need referral – sig. dec. in
compliance with HAART Demoralization – different from depression in
that it doesn’t have anhedonia◦ Need referral for counselling
AIDS mania - late◦ Present in manic state with no history of previous
disorders◦ Associated with cognitive impairment (AIDS
dementia)◦ R/O meningoencephalitis, need CT, LP
NNRTs can cause a psychosis, nightmares and increased irritability – within first four weeks of therapy◦ need to terminate med only for psychosis, the
other symptoms will resolve
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MSK/Rheumatologic MSK/Rheumatologic DiseaseDisease
- Old: HIV – associated arthritis/polymyositis
- Now: Osteoporosis and osteonecrosis most common (usually of the hip)- Think chronic recurrent pain of hip - > surgical
- With HAART increased incidence of infectious complications – septic arthritis, osteomyeltits, diskitis)
- In HAART era, immune syndrome caused by ARV’s has led some patients to develop sarcoidosis (mean time 9 months of therapy)- Symptomatic rx with corticosteroids
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OpthoOpthoCMV retinitis reduced by 80%
since onset of HAART therapyAny HIV + patient with any visual
loss or any macular edema needs urgent optho referral
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A Quick Primer on A Quick Primer on Needlestick InjuriesNeedlestick Injuries
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Hypothetical case:You’re at the end of your shift
and one of your resident collegues pulls you aside in the hallway (let’s call him….I dunno….Kris McKrossin…..with a K)
He tells you that he poked himself in the finger while putting in a central line on a patient a few hours ago and is wondering if he needs post-exposure prophylaxis.
What do you tell “Kris”?
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If you don’t know, ask!If you don’t know, ask!Report all casesOH & S Call line 234-7799
◦24 hrs a day/7 days a week
Ask the charge nurse◦Every ED has a pre-printed protocol
on what to do in case of exposures and access to PEP starter kit
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If you do get If you do get poked/exposedpoked/exposedRemove the contaminated clothes –
undergarments exceptedAllow immediate bleeding of the
woundWash the injured area well with
soap and water, and apply an antiseptic
If the eyes, nose, or mouth are involved, flush them well with large amounts of water
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Southern Alberta Clinic Southern Alberta Clinic GuidelinesGuidelines
1 Is the source known HIV+?◦ Yes: proceed to step 2 of protocol◦ No:
Test source (with consent) using rapid point-of-care HIV test available through CLS at any Emergency Room or Chumir Centre
If negative, and no risk of “window period”, reassure patient
If source unknown or refuses testing and has risks for or symptoms of HIV, proceed to step 2 of protocol
Consider source testing for HBV, HCV – most guidelines suggest testing for this
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Rapid HIV TestingRapid HIV Testing Sensitivity and Specificity both >90% Done in the on-site rapid response labs Current turn around time 1 hr 24 min – can take
about 4 hrs from blood draw to get result Realistically takes about 24hrs unless in special
circumstances Confirmed by Western Blot at Prov Lab Consider giving dose of PEP before results arrive
(based on your pre-test probability) CDC now endorsing more liberal use of rapid
point-of-care testing
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Southern Alberta Clinic Southern Alberta Clinic GuidelinesGuidelines
2 Timing and Type of Exposure:◦ Assess fluid type, volume, viral titre,
mode of exposure◦ Assess exact timing of exposure◦ If exposure is not considered
infectious for HIV/HBV/HCV (i.e. vomit, feces, etc. without blood –) reassure and arrange f/u if patient desires
◦ If exposure considered potentially infections go to 3
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3 Decision:◦ Make a decision for or against PEP
based on risk assessment (these are debatable) HIV + = start PEP HIV – and no risk of source pt being in
“Window period” = don’t start PEP Unknown (source not tested or refuses
testing) = evaluate risk (OHS and protocols binder)
Southern Alberta Clinic Guidelines
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Risk AssessmentRisk Assessment-Done by EP / OHS – guidance in protocols and -Done by EP / OHS – guidance in protocols and PEP kitPEP kit
High risk◦ IVDU◦ High risk sexual
behaviour (MSM, sex w/IVDU, multiple sexual partners (3 or more sexual partners/yr w/I past 5 yrs), prostitution
◦ Blood transfusion prior to 1985
◦ Sex w/HIV + person◦ Clinical suspicion of HIV
infections by physicians Prior HIV test HIV as part of a Ddx Unexplained
opportunistic infections (i.e. PCP, toxo, crypto, histo, TB, MAC)
Low Risk◦ HIV -◦ Serology unknown but
answers no to all high risk questions
Unknown◦ Source is not assessed
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4 Drug Selection Best to start within 1-2 hrs, consider dose before Rapid
HIV test returns depending on risk of source patient CHR has PEP kits prepared for us Basic Regimen:
◦ If Low risk exposure (unknown source or mucocutaneous exposure)
◦ Combivir: (AZT 300mg + 3TC 150mg) bid Expanded Regimen:
◦ For most percutaneous to known HIV + IN CONTACT WITH ID
◦ Basic Regimen + Nelfinavir 1250mg bid Other:
◦ consider other drugs if source patient is already on antiretrovirals or if source patient is known to have resistant HIV
Southern Alberta Clinic Guidelines
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Southern Alberta Clinic Southern Alberta Clinic GuidelinesGuidelines
5 Duration of Prophylaxis:◦Start ASAP and continue for 4 weeks
6 Discuss adverse reactions w/patient
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ED physician to order baseline CBC, diff., ALT
HBV, HCV, HIV serology
Follow up?
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Follow UpFollow UpOccupational exposures are sent
to Odyssey Travel and Tropical Medicine Clinic – 14th ST NW – Dr. Rudy Zimmer
Employee to make own appointment – phone # in the ED
MD to fax referral form to Dr. Zimmer
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ReferencesReferences Venkat et al. Care of the HIV-Positive Patient in the Emergency
Department in the Era of Highly Active Antiretroviral Therapy. Ann Emerg Med. 2008; 52:274-285
Rothman et al. Preventive Care in the Emergency Department: Should Emergency Departments Conduct Routine HIV Screening? Acad Emerg Med 2003; 10; 278- 285.
Rothman et al. HIV and complications in Emergency Medicine. Emerg Med Clin N Am 2008; 26; 367-387.
Emergency Med Reports HIV Positive Patient in the ED Part I and II, Vol 27:9, Apr. 2006
FMC ED Charge Nurse Manual (PDF File) Management of Health Care workers exposed to HIV.
www.uptodate.com When to Initiate Antiretroviral therapy in HIV-infected patients
www.uptodate.com Primary HIV-1 Infection: Diagosis and Treatment
www.uptodate.com Tintinalli, J. Emergency Medicine: A comprehensive study guide 6th
Ed. 2004. pgs. 925-935. Google Images Dr. Margriet Gredanus and Dr. James Huffman